Over-expression of Wild-type p53-induced phosphatase 1 confers poor prognosis of patients with gliomas

Liang, Chaohui; Guo, Erkun; Lü, Shan; Wang, Shuai; Kang, Chunsheng; Chang, Liang; Liu, Liqiang; Zhang, Guangyu; Wu, Zhiyong; Zhao, Zongmao; Ma, Shenglin; Wang, Liqun; Jiao, Baohua

doi:10.1016/j.brainres.2011.12.052

Cited by 22 publications

(12 citation statements)

References 26 publications

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“… 215 ). These data suggest a possible novel therapeutic approach for tumours expressing high levels of WIP1 and with activated HH pathway, such as a subset of MB, gliomas and melanomas (Refs 215 , 293 , 294 , 295 ). Targeting WIP1 in tumours with wild type p53 would lead not only to restoration of p53 tumour suppressor activity (Ref.…”

Section: Evidence For Rational Combinationsmentioning

confidence: 91%

Cooperative integration between HEDGEHOG-GLI signalling and other oncogenic pathways: implications for cancer therapy

Pandolfi

Stecca

2015

Expert Rev. Mol. Med.

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The HEDGEHOG-GLI (HH-GLI) signalling is a key pathway critical in embryonic development, stem cell biology and tissue homeostasis. In recent years, aberrant activation of HH-GLI signalling has been linked to several types of cancer, including those of the skin, brain, lungs, prostate, gastrointestinal tract and blood. HH-GLI signalling is initiated by binding of HH ligands to the transmembrane receptor PATCHED and is mediated by transcriptional effectors that belong to the GLI family, whose activity is finely tuned by a number of molecular interactions and post-translation modifications. Several reports suggest that the activity of the GLI proteins is regulated by several proliferative and oncogenic inputs, in addition or independent of upstream HH signalling. The identification of this complex crosstalk and the understanding of how the major oncogenic signalling pathways interact in cancer is a crucial step towards the establishment of efficient targeted combinatorial treatments. Here we review recent findings on the cooperative integration of HH-GLI signalling with the major oncogenic inputs and we discuss how these cues modulate the activity of the GLI proteins in cancer. We then summarise the latest advances on SMO and GLI inhibitors and alternative approaches to attenuate HH signalling through rational combinatorial therapies.

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Section: Evidence For Rational Combinationsmentioning

confidence: 91%

Cooperative integration between HEDGEHOG-GLI signalling and other oncogenic pathways: implications for cancer therapy

Pandolfi

Stecca

2015

Expert Rev. Mol. Med.

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“…On the other hand, tumors that retain wild-type p53 are likely to accumulate other genetic defects that would allow them to overcome the DDR barrier, providing a growth advantage in the presence of replicative stress. Importantly, amplification of the 17q23 locus carrying the PPM1D gene has been reported in various p53 wild-type tumors, pointing toward a role of Wip1 in cancer development, and Wip1 overexpression is associated with poor prognosis (Bulavin et al, 2002(Bulavin et al, , 2004Li et al, 2002;Saito-Ohara et al, 2003;Rauta et al, 2006;Castellino et al, 2008;Liang et al, 2012). The oncogenic behavior of Wip1 is further supported by mouse genetics showing that loss of Wip1 protects from cancer development (Bulavin et al, 2004;Nannenga et al, 2006).…”

Section: Introductionmentioning

confidence: 97%

Gain-of-function mutations of PPM1D/Wip1 impair the p53-dependent G1 checkpoint

Kleiblová

Shaltiël

Benada

et al. 2013

Journal of Cell Biology

141

148

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“…C-reactive protein, interleukin-6 (IL-6), and tumor necrosis factor-alpha) [20]. Numbers of studies have confirmed that chronic inflammation can stimulate the proliferation of glial cells, which is the one of the major components of ERMs in PDR [21, 22]. Therefore, the proliferation of glial cells and inflammation might be the important points of penetration to explore the pathogenesis of ERM after PDR.…”

Section: Discussionmentioning

confidence: 99%

Expression of wild-type p53-induced phosphatase 1 in diabetic epiretinal membranes

Zhong

Cui

et al. 2017

Oncotarget

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ObjectiveThe aims of the present study were to investigate the expression and distribution of Wild-type p53-induced phosphatase 1 (Wip1) in diabetic patients with proliferative diabetic retinopathy (PDR) with epiretinal membranes (ERMs) meanwhile analyze the colocalization of Wip1 and nuclear factor kappa-B (NF-κB) p65 in ERMs.MethodsERMs samples were collected from patients with PDR (PDR group) or non-diabetic patients with idiopathic epiretinal membranes (iERMs) (control group) during pars plana vitrectomy. Real-Time PCR analysis was carried out to examine the mRNA expression of Wip1 in ERMs. Immunohistochemical analysis and Immunofluorescent analysis were performed to detect the protein expression of Wip1 in ERMs. Double immunofluorescent staining was performed to detect the colocalization of Wip1 and glial fibrillary acidic protein (GFAP) (retinal glial cells marker), also Wip1 and NF-κB.ResultsERMs were obtained from 17 eyes of 17 patients with PDR (the PDR group) and 9 eyes of 9 nondiabetic patients (the control group) with iERMs. Our results showed high expression levels of Wip1 mRNAs in ERMs after PDR, but low in iERMs. In addition, both immunohistochemistry and immunofluorescence assay showed strong immunoreactivity for Wip1 in PDR ERMs. Furthermore, Wip1 and GFAP were coexpressed in PDR membranes. Finally, the expression of Wip1 was paralleled with NF-κB.ConclusionThese data support the notion that Wip1 contributes to the formation of the ERMs in PDR membranes via NF-κB signaling.

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Over-expression of Wild-type p53-induced phosphatase 1 confers poor prognosis of patients with gliomas

Cited by 22 publications

References 26 publications

Cooperative integration between HEDGEHOG-GLI signalling and other oncogenic pathways: implications for cancer therapy

Cooperative integration between HEDGEHOG-GLI signalling and other oncogenic pathways: implications for cancer therapy

Gain-of-function mutations of PPM1D/Wip1 impair the p53-dependent G1 checkpoint

Expression of wild-type p53-induced phosphatase 1 in diabetic epiretinal membranes

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